% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Shen:130557,
      author       = {Z. Shen and Y. Liu and B. Dewidar and J. Hu and O. Park and
                      T. Feng and C. Xu and C. Yu and Q. Li and C. Meyer and I.
                      Ilkavets and A. Müller and C. Stump-Guthier and S. Munker
                      and R. Liebe and V. Zimmer and F. Lammert and P. R. Mertens
                      and H. Li and P. Ten Dijke and H. Augustin$^*$ and J. Li and
                      B. Gao and M. P. Ebert and S. Dooley and Y. Li and H.-L.
                      Weng},
      title        = {{D}elta-{L}ike {L}igand 4 {M}odulates {L}iver {D}amage by
                      {D}own-{R}egulating {C}hemokine {E}xpression.},
      journal      = {The American journal of pathology},
      volume       = {186},
      number       = {7},
      issn         = {0002-9440},
      address      = {New York [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2017-05636},
      pages        = {1874 - 1889},
      year         = {2016},
      abstract     = {Disrupting Notch signaling ameliorates experimental liver
                      fibrosis. However, the role of individual Notch ligands in
                      liver damage is unknown. We investigated the effects of
                      Delta-like ligand 4 (Dll4) in liver disease. DLL4 expression
                      was measured in 31 human liver tissues by
                      immunohistochemistry. Dll4 function was examined in carbon
                      tetrachloride- and bile duct ligation-challenged mouse
                      models in vivo and evaluated in hepatic stellate cells,
                      hepatocytes, and Kupffer cells in vitro. DLL4 was expressed
                      in patients' Kupffer and liver sinusoidal endothelial cells.
                      Recombinant Dll4 protein (rDll4) ameliorated hepatocyte
                      apoptosis, inflammation, and fibrosis in mice after carbon
                      tetrachloride challenge. In vitro, rDll4 significantly
                      decreased lipopolysaccharide-dependent chemokine expression
                      in both Kupffer and hepatic stellate cells. In bile duct
                      ligation mice, rDll4 induced massive hepatic necrosis,
                      resulting in the death of all animals within 1 week.
                      Inflammatory cell infiltration and chemokine ligand 2 (Ccl2)
                      expression were significantly reduced in rDll4-receiving
                      bile duct ligation mice. Recombinant Ccl2 rescued bile duct
                      ligation mice from rDll4-mediated death. In patients with
                      acute-on-chronic liver failure, DLL4 expression was
                      inversely associated with CCL2 abundance. Mechanistically,
                      Dll4 regulated Ccl2 expression via NF-κB. Taken together,
                      Dll4 modulates liver inflammatory response by
                      down-regulating chemokine expression. rDll4 application
                      results in opposing outcomes in two models of liver damage.
                      Loss of DLL4 may be associated with CCL2-mediated cytokine
                      storm in patients with acute-on-chronic liver failure.},
      keywords     = {Chemokine CCL2 (NLM Chemicals) / Chemokines (NLM Chemicals)
                      / Intracellular Signaling Peptides and Proteins (NLM
                      Chemicals) / Membrane Proteins (NLM Chemicals) / delta
                      protein (NLM Chemicals)},
      cin          = {A190 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27171900},
      pmc          = {pmc:PMC4929401},
      doi          = {10.1016/j.ajpath.2016.03.010},
      url          = {https://inrepo02.dkfz.de/record/130557},
}